This proposal is designed to clarify the contribution of behavioral life stressors and maladaptive coping patterns to the development of hypertension, a major health problem in the U.S. In Study 1, 60 men and women aged 18-45 still at risk for hypertension will undergo laboratory assessments of blood pressure and hemodynamic responses to standardized mental and physical stressors (including tasks where their role alternates between active versus passive coping). These lab assessments will be repeated 3 times: after placebo only, after nonselective beta-blockade, and after beta-blockade plus alpha-1 blockade, in a counterbalanced, double-blind protocol, to verify the role of specific sympathetic activity in mediating responses. Study 1 also includes 24-hour ambulatory blood pressure monitoring, to permit evaluation of the relationship between laboratory and real-life responses. It also includes an assessment of responses to treadmill exercise, and through Doppler echocardiography, comparisons of the relationships of blood pressure responses to physical stressors, lab mental stressors, and ambulatory life events to left ventricular mass index and diastolic dysfunction can be made. In Study 2, 40 men who had undergone ambulatory blood pressure monitoring as college students will undergo a follow-up assessment 3-4 years later as full-time workers including evaluation of responses to standardized stressors and 24- hours ambulatory monitoring. Thus, the predictive utility of ambulatory blood pressure data obtained in early adulthood may be tested. The predictive relationship of a self-focused pattern of coping with stress (self-blame, keep-to-self) will also be tested. In study 3, 80 men formerly studied as college students will undergo a 9-11 year follow-up, including assessment of blood pressure responses to standardized stressors and 24-hour ambulatory monitoring, plus echocardiographic determination of left ventricular mass index and diastolic dysfunction. This study will extend previous observations on the utility of cardiovascular stress responses as predictors of long-term increases in blood pressure and pathogenic changes in myocardial function.